(1) Background: Recently more and more Chinese clinical studies have been conducted to compare the efficacy and safety of roxadustat with erythropoiesis-stimulating agents (ESAs) in hemodialysis (HD) patients. We aimed to assess the efficacy and safety of roxadustat in Chinese HD patients. (2) Methods: The PubMed, Embase, the Cochrane Library, Web of Science, WanFang, China National Knowledge Infrastructure (CNKI), SinoMed, and VIP databases were searched from their inception to July 2022 for randomized controlled trials (RCTs) that compared the efficacy and safety of roxadustat to those of ESAs in treating anemia in Chinese HD patients. (3) Results: Twenty-one RCTs involving 1408 patients were enrolled. Our study showed that the improvement of hemoglobin (Hb) levels and iron metabolism were significantly higher in the roxadustat group than in the ESA group. Additionally, the total adverse events risk was significantly lower in the roxadustat group. (4) Conclusions: In this meta-analysis, we found that roxadustat was more effective and safer than ESAs in treating anemia in Chinese HD patients.

Soluble epoxide hydrolase (sEH) has previously been demonstrated to play an important part in kidney diseases by hydrolyzing renoprotective epoxyeicosatrienoic acids to their less active diols. However, little is known about the role of sEH in primary glomerular diseases. Here, we investigated the effects of sEH inhibition on proteinuria in primary glomerular diseases and the underlying mechanism. The expression of sEH in the renal tubules of patients with minimal change disease, IgA nephropathy, and membranous nephropathy was significantly increased. Renal sEH expression level was positively correlated with the 24 h urine protein excretion and negatively correlated with serum albumin. In the animal model of Adriamycin (ADR)-induced nephropathy, renal sEH mRNA and protein expression increased significantly. Pharmacological inhibition of sEH with AUDA effectively reduced urine protein excretion and attenuated renal pathological damage. Furthermore, sEH inhibition markedly abrogated the abnormal expressions of nephrin and desmin in glomerular podocytes induced by ADR. More importantly, AUDA treatment inhibited renal NF-κB activation and reduced TNF-α levels in rats with ADR-induced nephropathy. Overall, our findings suggest that sEH inhibition ameliorates renal inflammation and podocyte injury, thus reducing proteinuria and exerting renoprotective effects. Targeting sEH might be a potential strategy for the treatment of proteinuria in primary glomerular diseases.